Bovine viral diarrhea virus (BVDV) is a leading cause of enteric, respiratory and reproductive diseases in cattle, and is particularly associated with high morbidity and mortality rates in calves. There are more than 105 million cattle in the United States (USDA-NASS statistics, 2002) and the cattle industry accounts for approximately 40% of the total market value of U.S. agriculture (USDA, NASS statistics, 1999). Since endemic infections result in major economic loss, BVDV is considered a high priority disease of economic importance to U.S. animal agriculture.
While maternal antibodies protect neonatal calves and yearlings against wild-type (wt) BVDV infections, their high titers interfere with the efficacy of current BVDV vaccines. Thus, vaccination is normally delayed until the neutralizing maternal antibodies decay. Unfortunately, persistently infected (PI) calves are common in herds and yearlings become vulnerable to infection as BVDV-specific antibodies decline (12, 13, 15). Moreover, maternal antibodies do not adequately protect a significant proportion of neonatal calves—especially bull calves that fail to get sufficient amounts of colostrum on time.
What is needed is a vaccine capable of stimulating adaptive T cell immunity in neonatal calves in the presence of protective levels of colostrum-derived antibodies to facilitate the transition from transient passive immunity to acquired immunity without experiencing a period of vulnerability to BVDV infection.